Introduction
The aim of this chapter is to address the ques- tion: Where is the pain coming from in patellar tendinopathy? Although a traditional answer would be “inflammatory cells,” this is unlikely to be correct. In this chapter we first summarize the evidence that overuse patellar tendon injury (henceforth called patellar tendinopathy) is not primarily an inflammatory condition.1We then outline some noninflammatory mechanisms that may produce patellar tendon pain. This topic is clinically relevant because patient man- agement will be greatly simplified when we eventually understand what causes the pain of patellar tendinopathy.
Overuse Tendinosis – Not Tendinitis
It has been widely assumed that patellar tendon overuse caused inflammation, and therefore, pain. Despite the pervasiveness of this dogma, a large body of evidence contradicts this assump- tion.2-4It has become clear that the true cause of pain lies elsewhere: It may be mechanical dis- continuity of collagen fibers, biochemical irrita- tion that results from damaged tendon tissue activating nociceptors5,6or neovascularization.7 Alternatively, unique anatomical features may produce pain at the patellar tendon, such as impingement8or stress shielding.9
For many years, it was widely believed10that patellar tendinopathy had an inflammatory basis (Figure 15.1). Pain and inflammation have been linked since Celsus (AD14–37) reported the association of “rubor et tumor cum calor et dolor.”11,12 The clinical label “patellar ten-
donitis” implies that inflammation is present.
Furthermore, nonsteroidal and corticosteroidal anti-inflammatory agents are popular treatment modalities. Ultrasound13and magnetic resonance imaging14papers have reported the presence of
“inflammatory fluid” around symptomatic patellar tendons and thus reinforced this model.
As long ago as 1976, Giancarlo Puddu of Rome documented that the pathology in what was clin- ically known as “Achilles tendonitis” was separa- tion and fragmentation of collagen, which he labeled “tendinosis.”15 Since then, numerous authors have shown that tendinosis is the pre- dominant pathology in patellar tendinopathy4 and these findings are briefly reviewed here and discussed in detail in the next chapter.
Macroscopically, the patellar tendon of patients with patellar tendinopathy contains soft, yellow-brown and disorganized tissue in the deep posterior portion of the patellar tendon adjacent to the lower pole of the patella.16-18This macroscopic appearance is often described as
“mucoid” degeneration.19,20 Under the light microscope, there is a loss of the normal tightly bundled parallel collagen fiber appearance;
instead fibers are in disarray and separated by increased ground substance. Collagen degener- ation with variable fibrosis and neovasculariza- tion was a consistent feature across studies.21
When imaging studies in athletes with patel- lar tendinopathy were correlated with histo- pathology, areas of hypoechogenicity on ultrasonography3and increased signal on MR imaging2,3 corresponded with collagen and mucoid degeneration.
257
15
Patellar Tendinopathy:
Where Does the Pain Come From?
Karim M. Khan and Jill L. Cook
Does a Short-term Inflammatory “Patellar Tendinitis” Precede the Noninflammatory Tendinosis?
Some consider that tendinosis is the end-stage of a continuum that begins with normal tendon and passes through a period of painful “tendi- nitis” (Figure 15.2). Although this is plausible, there is no evidence for a significant interim phase of “tendinitis” in overuse tendinopathy.
Data to explore this question comes from biopsy samples in athletes with patellar tendinopathy, biopsies taken in cases of patellar tendon rup- ture, and animal models of tendinopathy.
In our histopathological study of athletes who underwent surgery for jumper’s knee,3 several subjects were operated on after only 4 months of pain, and even in these cases inflammatory cells were absent. Patellar tendinopathy is thought to progress distally from the proximal pole with time, as the hypoechoic region enlarges.22Thus, we identified the proximal patellar attachment of the specimens obtained at surgery with a suture, and the histopathologist was able to carefully scrutinize the transition from abnor- mal to normal3(Figure 15.3). If tendinitis were to always precede tendinosis, then this region
should contain evidence of tendinitis. However, there were no inflammatory cells at this transi- tion area, suggesting that if there is such a phase of tendinitis, it is rather brief.
Further human evidence for tendinosis aris- ing without a period of painful tendinitis comes from studies of tendon ruptures. Pekka Kannus and Laszlo Józsa examined tendon tissue in cases of spontaneous patellar tendon rupture and found preexisting degenerative tendon pathology (tendinosis) at sites near, but distinct from, the rupture even in patients who had never had any tendon symptoms.23 By deduc- tion, painful tendinitis is not a prerequisite for tendinosis.
There are no animal models of patellar tendinopathy but experiments causing overuse tendinopathy of the plantaris tendon and Achilles tendon provide important histopatho- logical specimens of tendon tissue soon after injury. This provides insight as to the length of any inflammatory tendinitis that precedes colla- gen degeneration.
In a rat plantaris tendinopathy model24ten- dons were examined at 1 and 2 weeks. At both these times there was no evidence of inflamma-
Inflammation ('tendinitis')
Pain fibers in collagen respond to inflammation
Pain can be decreased by inhibiting inflammation Implication
Normal tendon
'acute' inflammatory
tendinitis
'chronic' non- inflammatory
tendinitis
Figure 15.1. The classical “inflammatory” model of tendon pain.
Figure 15.2. Proposed transition from normal tendon, through “tendinitis,” to tendinosis.
tion but there was strong evidence of tendon repair, as quiescent fibroblasts had trans- formed into rounded, active cells. These cells were identical to those found in human overuse tendinopathy.
Backman and colleagues developed a rabbit model to study overuse Achilles tendinopathy using transcutaneous stimulation of the calf muscle.25 They reported degenerative collagen changes (“fibrillation”) and neovascularization, together with some inflammatory cells in the adipose tissue close to the paratenon. They con- sidered this histopathology to be “identical to those reported in biopsy material from profes- sional runners and joggers with sustained Achilles tendon complaints admitted for surgery after months or years of non-beneficial conser- vative management.”25
Chukuka Enwemeka from Kansas examined the issue of duration of tendon inflammation in a surgical tenotomy model.26 This surgical model is known to generate much more inflam- mation than an overuse model. In this experi- ment, rats had the Achilles tendon severed transversely and then reapproximated and sutured with three loops of 3/0 surgical silk.
The skin was closed and the limb immobilized.
This intervention produced a prominent inflam-
matory response that peaked at 5 days and disappeared by day 18. Thus, even in a model predicted to stimulate considerably more inflammation than an overuse injury model, inflammatory cells disappeared within 3 weeks of surgical insult. Although healing of rat ten- dons does not necessarily translate directly into healing in humans, these data suggest that inflammation is not a lengthy process in tendon repair, even after surgical tenotomy.
Thus, human and animal data downplay the role of inflammation in the pain of chronic patellar tendinopathy. Although there may be a period of inflammation for a few days after cer- tain tendon injuries, symptoms that are present for more than one week must arise from a non- inflammatory mechanism. Noninflammatory mechanisms that may explain pain include mechanical models (collagen separation, tissue impingement), neurovascular models (neovas- cularization), and biochemical models. These models are the focus of the rest of this chapter.
Can Noninflammatory Mechanisms of Tendon Pain Explain the Pain-relieving effect of Corticosteroid Injections?
We cannot exhort the reader to abandon the inflammatory model of chronic tendinopathy without discussing the effect of corticosteroid injections. One of the most frequent questions we are asked when presenting these histo- pathological findings in tendinopathy is “Why do corticosteroids work?” Whether or not corti- costeroids benefit patients with tendinopathy is an issue that is the focus of other articles.27-32 Nevertheless, both clinical experience and ran- domized studies33,34 have shown these medica- tions provide at least short-term pain relief.
Also, the protease inhibitor aprotinin has been shown to relieve tendon pain.35
It has been postulated that any chemical agent (e.g., corticosteroids) may bathe the region of tendinosis and alter the chemical composition of the matrix (e.g., pH level).21 Fenestration of an area of tendinosis with needling may pro- mote beneficial bleeding into new channels cre- ated through degenerated mucoid tissue. This mechanical disruption may transform a failed intrinsic healing response into a therapeutic extrinsic one. At present, the mechanism of pain relief from these agents remains unknown – and this will likely remain the case until the mecha- nism of pain in tendinosis itself is understood.
Patella Stitch placed
in the proximal portion of the
tendon
Anterior view Posterior view
Figure 15.3. A method to examine histopathology of tendon tissue that may only recently have become abnormal. In patients who underwent patellar tendon surgery for chronic jumper’s knee, the abnormal tissue was excised completely as shown (dotted line) and a stitch of 4/0 silk was placed in the proximal portion so that the histopathologist could orient the specimen. It would be expected that the distal tendon tissue had become abnormal more recently than the proximal tendon as patellar tendinopathy normally extends distally from the proximal pole with time. Tendinosis diminished in severity with distance from the patella but there was no evidence of a transition zone of “tendinitis” at the bor- der between normal and abnormal tissue.3
Mechanical Models of Pain in Tendinopathy
Mechanical models of patellar tendon pain include those that attribute pain to damage to collagen fibers and those associated with tissue catching between the patella and the proximal tibia. We begin with theories of pain arising from collagen damage.
Collagen Fiber Disruption and Patellar Tendon Pain
This model is based on the premise that collagen fibers are pain free when intact and painful when disrupted (Figure 15.4). This is analogous to the mechanism of acute ligament sprain.
While nobody would deny that acute tearing of collagen causes pain (e.g., acute partial tendon tears), we have observed numerous situations where tendons are not completely intact, yet remain pain free. These observations are listed to highlight that tendon pain may not be due to a straightforward relationship between mechan- ical collagen separation and pain.
Observations about Tendon Pain and Surgical Findings
Two types of surgery performed on the patellar tendon – ACL autograft reconstruction and tenotomy for painful jumper’s knee – illuminate the relationship between collagen and tendon pain. Consider first the middle third patellar ten- don autograft ACL reconstruction. Individuals who undergo this operation have minimal donor site knee pain, yet collagen has been excised (Figure 15.5). Even at 2 years postoperatively, the donor site may have significant histological abnormality, yet remain pain free.36,37
Some would argue that completely excised collagen contains no intact fibers to produce pain, just as a complete ligament rupture is less painful than a substantial partial rupture.
Nevertheless, in the postoperative period some patients develop pain consistent with patellar tendinopathy, indicating that healing collagen can become painful.38 When imaged, the painful tendon donor site remains indistin- guishable from that in individuals who remain pain free.38,39 This indicates that the relation- ship between pain and collagen status is not one that can be detected at the macroscopic level.
Clinical observations in athletes undergoing surgery for jumper’s knee also provide thought- provoking data regarding collagen and pain. We monitored athletes recovering from open patel- lar tenotomy with both ultrasound (3 monthly) and MR imaging (6 monthly) for one year.40 Tendons remained largely abnormal to imaging, but this correlated poorly with pain. In a retro- spective study of a similar postoperative popula- tion, ultrasound imaging at a mean of 4 years also did not correlate with pain and function.41 Both of these studies confirm that even substan- tial degrees of collagen insult do not automati- cally produce tendon pain.
Jumper’s knee can also be treated by arthro- scopic debridement of the posterior border of the patellar tendon,42and this provides partic- ularly interesting evidence regarding the role of collagen defects in tendon pain. In this pro- cedure, the surgeon first debrides the adherent fat pad to expose the posterior aspect of the tendon (Figure 15.6) and then removes the cheesy, tendinosic tissue itself. The body of the tendon, however, remains largely untouched and postoperative ultrasonography reveals that the
Collagen separation (tendinosis, partial tears)
Pain fibers within tendon collagen respond to injury
Pain is related to collagen injury and repair Implication
Figure 15.4. The “mechanical” model of collagen separation causing tendon pain.
intratendinous hypoechoic region (so often con- sidered pathognomonic of this condition) is still evident, yet pain is significantly reduced.
This form of treatment could relieve pain by a number of mechanisms, including denervation.
However, the proportion of patients who reported skin paresthesia or numbness after patellar ten- don surgery was the same after arthroscopic or open patellar tenotomy, suggesting a similar degree of denervation in both anterior and poste- rior approaches to the patellar tendon.41
Longitudinal tenotomy is a well-established treatment for overuse tendinopathy at various body sites including the patellar tendon.43This causes new injury to tendon and, although the tenotomy is directed longitudinally so as not to sever the tendon, it is inevitable that collagen is divided because of the normal spiraling of ten- don. Nevertheless the procedure is often thera- peutic rather than deleterious. This phenomenon cannot be explained by invoking a purely mechanical model of pain in tendinopathy.
Observations about Tendon Pain and Imaging Appearances
A variant of the structural model of pain in tendinopathy outlined above argues that it is not torn collagen that hurts per se, but the persisting intact collagen that is placed under greater load because adjacent collagen is injured, and thus becomes painful. Pain is presumed to occur when the proportion of collagen injured reaches a critical threshold and persisting collagen is stressed beyond its normal capacity into a painful overload zone. This model predicts that greater degrees of tendinosis should be more painful than lesser degrees, until complete ten- don rupture, in which case pain disappears because there is no longer any collagen left under tension. Data from numerous imaging studies argue against this model.
In patients with patellar tendon pain, size of collagen abnormality as measured on ultrasound does not correspond with pain, either in cross- sectional studies44,45or in longitudinal observa- tional studies where change in area of abnormal tissue was monitored.22 Patients with patellar tendinopathy can also have a normal MR scan.46 This is seen in clinical practice where a patient may have a very small, or no, morphological abnormality, yet have significant symptoms.
In parallel studies conducted in large num- bers of asymptomatic athletes, ultrasonographic
Vastus medialis
Sartorius
Tibial tubercle Iliotibial
band
Patellar tendon
Patella
Tibia
Patellar tendon Infrapatellar
fat pad Figure 15.5. The middle third of the patellar tendon is removed in auto- graft ACL reconstruction. Although a great deal of collagen is removed, the patient is generally pain free soon after the operation. Complete tendon regeneration takes up to two years, but morphology does not correspond with pain of patellar tendinopathy in those patients who develop it.
Figure 15.6. Arthroscopic debridement of the patellar tendon involves mainly excision of the fat pad adhering to the posterior aspect of the proximal patellar tendon near its junction with the patella. At surgery, the mucoid degeneration of the posterior portion of the patellar tendon is clearly evident as a cheesy adhesion to the normal tendon. Surgery does little to disturb the tendon itself, yet patients often report that their patellar tendon pain is absent postoperatively.
hypoechoic regions (abnormal collagen) were common, even in subjects with no past history of jumper’s knee.44,45,47Another study using MR imaging in asymptomatic controls found an abnormal signal consistent with collagen degen- eration.46 These examples demonstrate that there is more to tendon pain than discontinuity of collagen.
Tissue Impingement Causing Patellar Tendon Pain
Both the patellar tendon and the fat pad are in a position where they could be pinched between the patella and the proximal tibia. Could this be the cause of pain in patellar tendinopathy?
Impingement as a Mechanism of Patellar Tendon Pain
Impingement is a form of mechanical load, and adds compressive or shearing load to the ten- don’s normal tensile load. Johnson and col- leagues8 argued that tension failure of the patellar tendon would affect the superficial fibers more than the deep surface, which is not the case in patellar tendinopathy. Thus, they proposed an alternative mechanism of the pain and the lesion of jumper’s knee: impingement of the inferior pole of the patella on the patellar tendon during knee flexion (Figure 15.7).
Three clinical observations are inconsistent with deep knee flexion (and impingement) caus- ing jumper’s knee pain. First, pain commences in the early phase of landing from a jump, with quadriceps muscle contraction while the knee is still relatively extended. Second, patients with severe jumper’s knee have pain on muscle con- traction even when the knee is fully extended and unloaded (e.g., lying in bed), whereas patients with impingement syndromes generally obtain substantial relief when the joint is moved away from the impinging direction. Third, the pain of jumper’s knee does not disappear and may actually increase when palpation is per- formed with the knee in full extension.
A dynamic magnetic resonance study investi- gated this hypothesis48 and found there was no difference in patellar movement between symp- tomatic tendons and those tendons without pain and pathology. The angle of the tendon to the patella either with or without quadriceps contrac- tion was similar in both these groups, suggesting that impingement was not a causative factor.
Furthermore, Johnson’s argument that tension failure of the patellar tendon would affect the superficial fibers more than the deep surface is only valid if the superficial and deep fiber attach- ments are equally strong. Biomechanical studies, however, found the superficial attachment to be far stronger than the deep.49,50Thus, tension fail- ure can influence the deep fibers preferentially. In combination, clinical and research findings sug- gest that impingement from the patella may not be a factor in patellar tendinopathy.
Another theory more recently proposed by Louis Almekinders from North Carolina is the
“stress-shielding” theory.51,52The stress-shield- ing theory considers tendinopathy to be a com- bined overuse-underuse injury, where the superficial portion of the tendon bears too much of the tensile load while the deep portion of the tendon bears too little of the same load. Further investigation is required; however, it is clear that critical etiological questions such as the nature of tendon load must be answered quickly, as it is the essence of adequate management.
The Role of the Fat Pad in Patellar Tendon Pain
Duri53speculated that the fat pad has “an impor- tant role in the production of intense pain in
Figure 15.7. Illustration of the argument for an “impingement” model of pain in patellar tendinopathy. Assuming that the insertion of the patellar tendon to the patella was of a uniform strength, tension on the tendon with the knee flexed should generate more force superficially (large arrows) than deeply. Thus, an impingement model was proposed whereby pain, and pathology, was caused by the patellar impinging against the tendon tissue (see text).
patellar tendonitis” when it adheres to the back of the patellar tendon and causes “synovitis.”
The infrapatellar fat pad is an extremely sensi- tive region54,55with many nociceptors. However, surgical management of the main body of the patellar tendon in athletes revealed no macro- scopic abnormality of the fat pad.56Intuitively, one would be loath to attribute tendon symp- toms to a structure found only at one or two anatomical sites (i.e., the patellar fat pad, Kager’s triangle) when tendinopathy occurs at various sites. On the other hand, the fat pad may be a specific form of the nociceptive peritendi- nous tissue that is sensitive to biochemical irri- tants. That is, the fat pad in the patellar tendon may play the same role as the paratenon in Achilles tendinopathy and the subacromial bursa in rotator cuff tendinopathy.
Note that the fat pad undoubtedly plays a role in anterior knee pain independently of any role in patellar tendinopathy. Jenny McConnell, the Australian physiotherapist renowned for her work in patellofemoral pain syndrome,57recog- nized fat pad impingement as a cause of anterior knee pain (not necessarily tendon pain) over 10 years ago. Most clinicians would agree that some patients appear to suffer a chronic version of anterior knee pain aggravated by knee exten- sion, similar to the condition referred to as Hoffa’s syndrome, when presenting with acute trauma to the anterior knee.58
Biochemical Models of Pain in Tendinopathy
If one discards the inflammatory model of pain production, and has reservations about a purely mechanical model for the reasons listed above, the biochemical irritant model becomes increas- ingly attractive.6,21 (Figure 15.8). Bob Nirschl said, “We suspect that the cause of pain in tendi- nosis is chemical irritation due to regional anoxia and the lack of phagocytic cells to remove noxious products of cellular activity.”21 It may be that the pain of tendon overuse injury is largely due to biochemical factors activating peritendinous nociceptors.
The elusive noxious agent could include matrix substances and minor collagens that are only currently being characterized in normal tis- sues. For example, chondroitin sulphate exposed through tendon damage may stimulate nocicep- tors.6,30,59In the knee, nociceptors are located in the retinaculum, fat pad, synovium, and perios- teum,60and all these structures may play a role in the mechanism of pain in patellar tendinopathy.
In 39 cadaver dissections of the proximal patellar tendon,3we consistently identified a thin layer of fat adherent to the posterior portion of the patel- lar tendon. In the corresponding tissue speci- mens from patients operated on for chronic jumper’s knee, this fat tissue contained increased Alcian Blue stain (and thus, glycosaminoglycans)
Figure 15.8. A proposed “biochemical irritant” tendon pain model.
Yet unidentified biochemical irritants (candidates include matrix substances such as chondroitin sulphate) become exposed because of
collagen degeneration (tendinosis). Alternatively, excitatory neurotransmitters are exposed
Significant pain fibers are found in synovium and tissue around tendon, as well as in the tendon substance − Substance P may mediate pain
Implications
1. Tendon healing would reduce the concentration of biochemical irritants and thus, pain.
2. Pharmaceutical antidote to the biochemical irritants would decrease pain 4. Denervation of nociceptors (i.e., certain surgery) would decrease pain 3. Pharmaceutical antidote to substance-P may decrease pain
that had presumably extravasated from the adja- cent region of tendinosis.
Another potential candidate is glutamate, which has been recognized as a mediator of pain61 and has been demonstrated in several tendons of the body at significantly higher levels in pathological tendons than in normal ten- dons.5,62,63 Certain ionotropic glutamate recep- tors are present in unmyelinated and myelinated sensory axons,64 and glutamate antagonists reduced the pain that rats felt when given a test dose of formalin. Using in vivo microdialysis, Hakan Alfredson and colleagues63 found that the neurotransmitter glutamate was present in higher intratendinous concentrations in subjects with patellar tendinopathy than con- trols. However, their more recent studies have found that the levels of glutamate do not decrease in those tendons that become asympto- matic after eccentric exercise treatment,65 sug- gesting that glutamate is not as important as first thought with regard to mediating tendon pain.
Substance-P, and the related neuropeptide, calcitonin gene related peptide (CGRP), has also been found in nerve afferents around the feline knee66 and are thought to be involved in joint nociception.
A structural relationship has been observed between neuropeptide containing nerve fibers and collagen.66 However, how tendon injury is transduced into nerve impulses, and perhaps a pain signal, remains unclear. Although there are some data on innervation of tendon,30,67 and there is ultrastructural evidence of all four cate- gories of nerve endings (Ruffini corpuscles, Vater-Pacini corpuscles, Golgi tendon organs, and free nerve endings or pain receptors) in normal tendons,30this field requires a great deal more work before the mechanism of tendon pain is unraveled. If substance-P proved to be a significant agent in tendinopathy, its already developed nonpeptide antagonists could be appropriate for a therapeutic trial.68
Can the Biochemical Model Explain the Therapeutic Effect of Eccentric Tendon Strengthening?
The mechanism whereby eccentric strengthen- ing reduces tendon pain remains to be fully elu- cidated. Al Banes’s group at the University of North Carolina have used in vivo animal mod- els, intact tendon specimens and cell cultures to
investigate the relationship between mechanical loading and tenocyte response. These authors have provided seminal evidence that tenocytes communicate in response to mechanical load via gap junctions and the cytoskeleton within tenocytes.69-71It is therefore possible that eccen- tric strengthening may stimulate a positive ten- don response and therefore also potentially affect tendon pain. Although it is far too early to correlate these findings with the pain-reducing effect of eccentric strength programs, it is apparent that the painful training program that may initially increase, but then decrease, the pain of Achilles and patellar tendinopathy72-74 may provide the type of mechanical stimulus that Banes has shown promotes DNA and colla- gen production. Banes’s model, and the data that underpin it, is consistent with the clinical evidence that tendon repair can be stimulated by mechanical loading, without a need to invoke any inflammatory pathways. The interested reader is directed to the referenced papers for detailed explanation of the pathway between mechanical stimulus and collagen production in tendon.75
Clinical Implications if Pain Were Due to Biochemical Irritants
If the “biochemical irritant” model of tendon pain proves to have some validity, it would mean that clinical management would aim to modify the biochemical milieu. Collagen repair would, of course, contribute to resolving tendinopathy, but researchers would be encour- aged to pursue a pharmaceutical approach focused on reducing the irritant (but not neces- sarily inflammatory) biochemical compounds around the tendon.
Neural and Vascular Models of Pain in Tendinopathy
Normal tendons have a low vascularity, but have sufficient supply for their metabolic needs. In the pathological tendon, increases in vascularity (neovascularization) have been demonstrated histopathologically,21 with imaging on Doppler ultrasound,7,76,77 and with laser flowmetry78,79 (Figure 15.9). Further investigations have demonstrated that neovascularization has been associated with pain and, furthermore, scleros- ing or obliterating the neovascularization decreases tendon pain.80
Neovascularization may be associated with nerve fibers,63 including those immunoreactive to substance P and CGRP.81 The association between pain and neovascularization is not absolute, as some studies demonstrate that ten- dons with neovascularization may not be painful.82,83 Conversely, pathological tendons without neovascularization may also be painful.
However, there is evidence that there is more pain in pathological tendons with neovascular- ization compared to pathological tendons with- out neovascularization.84 Longitudinal studies demonstrate that neovascularization may come and go, and the stimulus for this and the relation to pain is currently undefined 84a.
David Hart and colleagues at the University of Calgary have proposed that the close proximity between neural elements and tissue mast cells in tendon would permit the mast cell–neurite “unit”
to stimulate what they termed “neurogenic inflammation.”85 As paratenon is more highly innervated and vascularized than tendon itself, it has been proposed that neurotransmitters such as substance P can influence mast cell degranula- tion and secretory activity. Neural activity could be amplified, via a feedback mechanism, when mast cells release a panel of biologically active molecules that impact on vascular elements and fibroblasts. Theoretically, the mediators con- tained in mast cells such as cytokines and growth factors could influence a number of potentially pain-producing factors such as cellular edema and chemotaxis for inflammatory cells. The pro-
ponents of this mechanism argue that the release of low amounts of these mediators could be part of the normal regulatory system, while higher levels may contribute to the adaptive response of tissues.85
This type of “neurogenic inflammation” has been seen in various body tissues, although not proven in tendon. The authors refer to this as an
“endogenous inflammatory system,” in contrast to the “exogenous inflammatory system” com- posed of bloodborne cells generally associated with inflammation.85One criticism of this model as it stands is that mast cells are not prominent in tendon tissue. Nevertheless, the model may apply to paratenonitis, and it may explain the process of neovascularization in tendinosis.
Conclusions
There is little doubt that overuse tendinopathy is noninflammatory. Although collagen fiber injury is almost certainly involved in production of pain in tendinopathies, it may not fully explain the mechanism of tendon pain. Numerous obser- vations illustrate that there is no perfect correla- tion between collagen injury and pain.
Any model of the pain mechanism in patellar tendinopathy must be consistent with the fol- lowing observations:
● The pathology underlying tendinopathy is tendinosis.
● Abnormal tendon morphology on imaging con- fers a risk, but not a guarantee, of symptoms.
Figure 15.9. Color Doppler ultrasound of a 19-year-old volleyball player with chronic patellar tendinopathy. Note the neovascularization within the hypoechoic region of his patellar tendon.
● Various surgical treatments including longi- tudinal tenotomy and arthroscopic tendon debridement can alleviate pain without directly affecting pathological tissue.
● Medical treatment such as corticosteroid injection and aprotinin can relieve the pain quickly, but not necessarily permanently.
● Eccentric strength training is effective in pain relief and can promote tendon healing.
Ideally, the model would apply at numerous sites of the clinically relevant tendinopathies.
Currently, the cause of tendon pathology and pain is unknown. Experimental and clinical research is clarifying aspects of the aetiology of tendon pain and pathology but the relationship between them is still unclear. Until we discover the cause of patellar tendon pain, options for ameliorating tendon pain will remain limited.
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